Furukawa K, Yamasaki Y, Kizu A, Furukawa K, Katsume H, Ijichi H, Kitamura K
J Mol Cell Cardiol. 1983 Sep;15(9):595-602. doi: 10.1016/0022-2828(83)90269-9.
With electrophysiological methods, mechanisms of the restorative action of coenzyme Q10 (CoQ10) in 2,4-dinitrophenol-depressed electrical and mechanical activities of isolated guinea-pig hearts were studied. Isoproterenol (3 X 10(-8) M)-induced action potential and contraction of the heart in 27 mM KCl Tyrode solution were abolished by 6 X 10(-6) M 2,4-dinitrophenol, while the additional application of CoQ10 (50 micrograms/ml) restored both these activities of the heart. This restorative action of CoQ10 was dose related (2 to 50 micrograms/ml) and was inhibited by 10 micrograms/ml 15-hydroperoxyarachidonic acid (15-HPAA) or pretreatment of the animals with indomethacin (5 mg/kg i.v.). When exogenously applied, 200 ng/ml prostacyclin also restored the 2,4-dinitrophenol-depressed electrical and contractile activities of the heart, but this restorative action of prostacyclin was affected neither by 15-HPAA nor by indomethacin pretreatment. These results suggest the possible participation of prostacyclin in the restorative action of CoQ10 in 2,4-dinitrophenol-depressed electrical and mechanical activities of the heart.
采用电生理方法,研究了辅酶Q10(CoQ10)对2,4-二硝基苯酚抑制的豚鼠离体心脏电活动和机械活动的恢复作用机制。在27 mM KCl Tyrode溶液中,6×10(-6) M 2,4-二硝基苯酚可消除异丙肾上腺素(3×10(-8) M)诱导的心脏动作电位和收缩,而额外添加CoQ10(50微克/毫升)可恢复心脏的这两种活动。CoQ10的这种恢复作用呈剂量相关(2至50微克/毫升),并被10微克/毫升15-氢过氧花生四烯酸(15-HPAA)或用吲哚美辛(5毫克/千克静脉注射)预处理动物所抑制。当外源性应用时,200纳克/毫升前列环素也可恢复2,4-二硝基苯酚抑制的心脏电活动和收缩活动,但前列环素的这种恢复作用既不受15-HPAA影响,也不受吲哚美辛预处理影响。这些结果提示前列环素可能参与了CoQ10对2,4-二硝基苯酚抑制的心脏电活动和机械活动的恢复作用。